ArticleCurrent biology : CB2016
H-ras Inhibits the Hippo Pathway by Promoting Mst1/Mst2 Heterodimerization.
Article in Current biology : CB, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- MISP Suppresses Ferroptosis via MST1/2 Kinases to Facilitate YAP Activation in Non-Small Cell Lung Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- MST1 interactomes profiling across cell death in esophageal squamous cell carcinoma.Medical review (2021) · 2024Article
- MST2 methylation by PRMT5 inhibits Hippo signaling and promotes pancreatic cancer progression.The EMBO journal · 2023Article
- Mutated HRAS Activates YAP1-AXL Signaling to Drive Metastasis of Head and Neck Cancer.Cancer research · 2023Article
- Protocol for visualizing conditional interaction between transmembrane and cytoplasmic proteins.STAR protocols · 2021Article
- Regulation of MST complexes and activity via SARAH domain modifications.Biochemical Society transactions · 2021Review
- Increasing kinase domain proximity promotes MST2 autophosphorylation during Hippo signaling.The Journal of biological chemistry · 2020Article
- Concerted localization-resets precede YAP-dependent transcription.Nature communications · 2020Article
- Hippo/Mst signaling coordinates cellular quiescence with terminal maturation in iNKT cell development and fate decisions.The Journal of experimental medicine · 2020Article
- Macrophage achieves self-protection against oxidative stress-induced ageing through the Mst-Nrf2 axis.Nature communications · 2019Article
- Detection of Heterodimerization of Protein Isoforms Using an in Situ Proximity Ligation Assay.Journal of visualized experiments : JoVE · 2018Article
- Hras helps hippo heterodimerize to evade tumor suppression.Small GTPases · 2018Review
- Fascin induces melanoma tumorigenesis and stemness through regulating the Hippo pathway.Cell communication and signaling : CCS · 2018Article
- Tumor suppressor C-RASSF proteins.Cellular and molecular life sciences : CMLS · 2018Review
- MST1 Suppression Reduces Early Brain Injury by Inhibiting the NF-Behavioural neurology · 2018Article
- NUP37, a positive regulator of YAP/TEAD signaling, promotes the progression of hepatocellular carcinoma.Oncotarget · 2017Article
- MiR-3910 Promotes the Growth and Migration of Cancer Cells in the Progression of Hepatocellular Carcinoma.Digestive diseases and sciences · 2017Article
- Article
- MST1/MST2 Protein Kinases: Regulation and Physiologic Roles.Biochemistry · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
The protein kinases Mst1 and Mst2 have tumor suppressor activity, but their mode of regulation is not well established. Mst1 and Mst2 are broadly expressed and may have certain overlapping functions in mammals, as deletions of both Mst1 and Mst2 together are required for tumorigenesis in mouse models [1-3]. These kinases act via a three-component signaling cascade comprising Mst1 and Mst2, the protein kinases Lats1 and Lats2, and the transcriptional coactivators Yap and Taz [4-6]. Mst1 and Mst2 contain C-terminal SARAH domains that mediate their homodimerization as well as heterodimerization with other SARAH domain-containing proteins, which may regulate Mst1/Mst2 activity. Here we show that, in addition to forming homodimers, Mst1 and Mst2 heterodimerize in cells, this interaction is mediated by their SARAH domains and is favored over homodimers, and these heterodimers have much-reduced protein kinase activity compared to Mst1 or Mst2 homodimers. Mst1/Mst2 heterodimerization is strongly promoted by oncogenic H-ras, and this effect requires activation of the Erk pathway. Cells lacking Mst1, in which Mst1/Mst2 heterodimers are not possible, are resistant to H-ras-mediated transformation and maintain active hippo pathway signaling compared to wild-type cells or cells lacking both Mst1 and Mst2. Our results suggest that H-ras, via an Erk-dependent mechanism, downregulates Mst1/Mst2 activity by inducing the formation of inactive Mst1/Mst2 heterodimers.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.